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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 09 Dec 2014.

Ataxia telangiectasia mutated homolog

serine/threonine protein kinase; critical regulator of the cellular DNA damage response [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: p53, CAN, V1a, HAD, p21
Papers on Atm
Enhanced susceptibility of ovaries from obese mice to 7,12-dimethylbenz[a]anthracene-induced DNA damage.
Keating et al., Ames, United States. In Toxicol Appl Pharmacol, 01 Jan 2015
Total ovarian RNA and protein were isolated and abundance of Ataxia telangiectasia mutated (Atm), X-ray repair complementing defective repair in Chinese hamster cells 6 (Xrcc6), breast cancer type 1 (Brca1), Rad 51 homolog (Rad51), poly [ADP-ribose] polymerase 1 (Parp1) and protein kinase, DNA-activated, catalytic polypeptide (Prkdc) were quantified by RT-PCR or Western blot.
p57Kip2 is an unrecognized DNA damage response effector molecule that functions in tumor suppression and chemoresistance.
Li et al., Shanghai, China. In Oncogene, Oct 2014
Genotoxic stress induces p57Kip2 expression via the bone morphogenetic protein-Smad1 and Atm-p38MAPK-Atf2 pathways in p53-proficient or -deficient cells and requires the Smad1-Atf2 complex that facilitates their recruitment to the p57Kip2 promoter.
Functional kinomics identifies candidate therapeutic targets in head and neck cancer.
Méndez et al., Seattle, United States. In Clin Cancer Res, Sep 2014
EXPERIMENTAL DESIGN: RNAi kinome viability screens were performed on HNSCC cells, including autologous pairs from primary tumor and recurrent/metastatic lesions, and in parallel on murine squamous cell carcinoma (MSCC) cells derived from tumors of inbred mice bearing germline mutations in Trp53, and p53 regulatory genes: Atm, Prkdc, and p19(Arf).
Radiation and ATM inhibition: the heart of the matter.
Muschel et al., In J Clin Invest, Sep 2014
Numerous in vitro studies have shown that human cell lines lacking functional ATM are extremely radiosensitive.
Atm deletion with dual recombinase technology preferentially radiosensitizes tumor endothelium.
Kirsch et al., In J Clin Invest, Sep 2014
Kinase inhibitors of ATM, the gene mutated in ataxia telangiectasia, can sensitize tumor cells to radiation therapy, but concern that inhibiting ATM in normal tissues will also increase normal tissue toxicity from radiation has limited their clinical application.
Anthracyclines induce DNA damage response-mediated protection against severe sepsis.
Moita et al., Lisbon, Portugal. In Immunity, Dec 2013
This salutary effect is strictly dependent on the activation of DNA damage response and autophagy pathways in the lung, as demonstrated by deletion of the ataxia telangiectasia mutated (Atm) or the autophagy-related protein 7 (Atg7) specifically in this organ.
Expression pattern of ataxia telangiectasia mutated (ATM), p53, Akt, and glycogen synthase kinase-3β in the striatum of rats treated with 3-nitropropionic acid.
Pelegrí et al., Barcelona, Spain. In J Neurosci Res, 2012
We examined whether cellular expression of ataxia telangiectasia mutated, p53, Akt, and glycogen synthase kinase-3beta, were involved in the striatal neurodegeneration in the brains of rats
Pathological neoangiogenesis depends on oxidative stress regulation by ATM.
Kubota et al., Tokyo, Japan. In Nat Med, 2012
The ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), acts as a barrier to cellular senescence and tumorigenesis.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
Bulavin et al., Singapore, Singapore. In Cell Metab, 2012
Here, we show that Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice; specifically, Wip1 deficiency prevents both conditions.
Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia.
Herrup et al., United States. In Nat Med, 2012
Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.
ATM controls meiotic double-strand-break formation.
Keeney et al., New York City, United States. In Nature, 2011
Here we report that the number of meiotic DSBs in mouse is controlled by ATM, a kinase activated by DNA damage to trigger checkpoint signalling and promote DSB repair.
Cytoplasmic ATM protein kinase: an emerging therapeutic target for diabetes, cancer and neuronal degeneration.
Burn et al., Sioux Falls, United States. In Drug Discov Today, 2011
The gene mutated in this disease, Atm (A-T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein controlling cell-cycle progression.
Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.
Pearson et al., Dundee, United Kingdom. In Nat Genet, 2011
ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin
Mdm2 links genotoxic stress and metabolism to p53.
Li et al., Shanghai, China. In Protein Cell, 2010
Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related).
p53 control of bone remodeling.
Li et al., Shanghai, China. In J Cell Biochem, 2010
Moreover, Atm, c-Abl, and Mdm2, upstream regulators of p53 in DNA damage response, regulate osteoblast differentiation and bone remodeling as well.
ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation.
Camins et al., Barcelona, Spain. In J Cell Biochem, 2010
These data demonstrate how a new molecular network on ATM regulates the cell cycle through the control of pRb phosphorylation.
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage.
Frisan et al., Stockholm, Sweden. In Plos One, 2009
data demonstrate that MYC contributes to the activation of the ATM-dependent checkpoint responses, leading to cell death in response to specific genotoxic stimuli
The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1.
Chapple et al., London, United Kingdom. In Hum Mol Genet, 2009
Sacsin knockdown resulted in a reduction in cells expressing polyglutamine-expanded ataxin.
Rad3 and Sty1 function in Schizosaccharomyces pombe: an integrated response to DNA damage and environmental stress?
Sunnerhagen et al., Göteborg, Sweden. In Mol Microbiol, 2008
In Schizosaccharomyces pombe, the Ataxia Telangiectasia-mutated (Atm)/Atm and Rad 3 Related (Atr) homologue Rad3 is an essential regulator of the response to DNA damage and stalled replication forks.
ATM activation and DNA damage response.
Kozlov et al., Brisbane, Australia. In Cell Cycle, 2007
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and cellular phenotype of A-T that this gene would play a central role in the DNA damage response.
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